In recent years, risks of death in coronary diseases such as myocardial infarction have increased with changes in life styles (Non-patent Document 1 or 2). Therefore, a method of diagnosing a critical risk for any of those diseases at an early stage has been expected to be developed.
The possibilities of development of coronary diseases such as myocardial infarction due to genetic predispositions have been suggested in the art. Several methods of diagnosing myocardial infarction on the basis of the presence or absence of a gene mutation have been known in the art. For instance, a method of diagnosing a risk of the onset of myocardial infarction by analyzing the polymorphism of a prostacyclin synthase gene has been known (Patent Document 1). However, for diagnosing more precisely, another method for the diagnosis has been expected to be developed.
A leptin receptor is a single-spanning membrane receptor that transmits a signal of leptin that is involved in regulation of food intake and energy expenditure (Non-patent Document 3). It has been known that polymorphisms in some regions of a gene encoding leption receptor are associated with metabolic diseases such as obesity (Non-patent Document 3). Polymorphisms in several portions of a gene that encodes the leptin receptor have been known to relate to asthma (a polymorphism that replaces Q with R: Non-patent Document 4). However, there is no finding with respect to the relationship between the polymorphism of the leptin receptor gene and inflammatory diseases such as myocardial infarction.
Galectins are proteins having affinities for galactose. In mammals, at present, 10 different galectins are known. Among those, galectin-2 is known to form a noncovalent homodimer composed of a 14 KDa subunit and it is self-aggregated to lose its activity in the absence of a reducing agent. In addition, the details of physiological functions of galectin-2 have not been known even though in many cases the expression of galectin-2 is found in epithelial cells in normal adult human tissues, mainly in the lower part of the small intestine (Non-patent Document 5).    Patent Document 1: JP2002-136291    Non-patent Document 1: Nature Medicine, 1997, vol. 3, p 600-601    Non-patent Document 2: New England Journal of Medicine, 1997, vol. 337, p 1360-1369    Non-patent Document 3: Cell, 1995, vol. 83, p 1263-1271    Non-patent Document 4: Hum Genet., 2001, vol. 108(3), p 233-236    Non-patent Document 5: Trends in Glycoscience and Glycotechnology, 1997, vol. 9, No. 45, p 87-93